Chapter 68
Acute Myeloid Leukemia
Tracy Stokol,
Tracy Stokol
Search for more papers by this authorTracy Stokol,
Tracy Stokol
Search for more papers by this authorBook Editor(s):Marjory B. Brooks DVM, DACVIM,
Kendal E. Harr DVM, MS, DACVP,
Davis M. Seelig DVM, PhD, DACVP,
K. Jane Wardrop DVM, MS, DACVP,
Douglas J. Weiss DVM, PhD, DACVP,
Marjory B. Brooks DVM, DACVIM
Director, Comparative Coagulation Section
Animal Health Diagnostic Center, Cornell University, Ithaca, New York, USA
Search for more papers by this authorKendal E. Harr DVM, MS, DACVP
URIKA, LLC, Mukilteo, Washington, USA
Search for more papers by this authorDavis M. Seelig DVM, PhD, DACVP
Associate Professor, Clinical Pathology
Department of Veterinary Clinical Sciences, University of Minnesota, College of Veterinary Medicine, St. Paul, Minnesota, USA
Search for more papers by this authorK. Jane Wardrop DVM, MS, DACVP
Professor and Director, Clinical Pathology Laboratory
Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA
Search for more papers by this authorDouglas J. Weiss DVM, PhD, DACVP
Emeritus Professor
College of Veterinary Medicine, University of Minnesota, St. Paul, Minnesota, USA
Search for more papers by this authorFirst published: 04 March 2022
Summary
Acute myeloid leukemia (AML) is the most common type of leukemia in adult human beings, and, even with advances in genetic testing and genetically tailored therapy, the prognosis remains poor. AML involves the clonal expansion of myeloid stem cells, which can either minimally or partially differentiate down a particular myeloid lineage. Genetic defects, such as internal duplications, gene fusions, and point mutations, underlie the pathogenesis of AML. In human medicine, cytomorphologic assessment and phenotyping are essential components of diagnosis; however, genetic analysis has become commonplace and a required part of the diagnostic evaluation of AML. Based on the 2008 updated and 2016 revised WHO criteria, AML is classified into six different categories in human patients: AML with recurrent genetic abnormalities, AML with myelodysplasia-related changes, therapy-associated AML, AML-not otherwise specified, myeloid sarcoma, and myeloid proliferations related to Down's syndrome.
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